ライフサイエンスコーパス: DPP-4

1 these chemokines by Dipeptidyl Peptidase IV (DPP-4).

2 eta-glucosidase, and dipeptidyl peptidase-4 (DPP-4).

3 to exogenous tumor necrosis factor-alpha and DPP-4.

4 tagliptin reduced the serum concentration of DPP-4.

5 compounds with subnanomolar activity against DPP-4 (42b- 49b), that is, 4-fluorobenzyl-substituted co

6 yl peptidase-4 (DPP-4); hence, inhibition of DPP-4 activity enables yet another pathway for potentiat

7 sm for DPP-4 inhibitors is that they inhibit DPP-4 activity in peripheral plasma, which prevents the

8 ivation of GLP-1R signaling or inhibition of DPP-4 activity produces a broad range of overlapping and

9 Blood DPP-4 activity, glucagon-like peptide-1 (GLP-1) levels,

10 Vildagliptin fully inhibited DPP-4 activity, reduced GLP-1 clearance by 40%, and incr

11 rtal GLP-1 receptors; 2) inhibition of islet DPP-4 activity, which prevents inactivation of locally p

12 ical mechanisms include 1) inhibition of gut DPP-4 activity, which prevents inactivation of newly rel

13 with vildagliptin on dipeptidyl peptidase-4 (DPP-4) activity, glucagon-like peptide 1 (GLP-1) concent

14 Dipeptidyl peptidase 4 (DPP-4; also known as CD26), a transmembrane receptor exp

15 OPEP-UWM database was performed and obtained DPP-4 and ACE inhibitors as the predominant bioactive ac

16 ein-based microcapsules showed the strongest DPP-4 and alpha-amylase inhibition, indicating potential

17 ss degradation is prevented by inhibition of DPP-4 and perhaps NEP.

18 trials, along with the potential utility of DPP-4 and periostin as biomarkers of interleukin-13 path

19 Following post translational silencing of DPP-4 and upregulation of IL-27 in a diet-induced obesit

20 Dipeptidyl peptidase 4 (DPP-4) and neprilysin (NEP) rapidly degrade glucagon-lik

21 nzymatic cleavage by dipeptidyl peptidase-4 (DPP-4) and through renal clearance.

22 on protein (FAP) and dipeptidyl peptidase-4 (DPP-4) are highly homologous serine proteases of the pro

23 , a new inhibitor of dipeptidyl peptidase 4 (DPP-4), as compared with placebo in patients with type 2

24 orter 2 (GLUT2), and dipeptidyl peptidase 4 (DPP-4), as well as that of the putative differentiation

25 ctural modeling suggests that FAP Ala657 and DPP-4 Asp663 confer their contrasting effects on TSS by

26 Conversely, DPP-4 Asp663 stabilizes dipeptidyl peptidase substrate b

27 FAP Ala657, which corresponds to DPP-4 Asp663, is important for endopeptidase activity; h

28 on of villin by 29% (6%), Cdx2 by 31% (10%), DPP-4 by 15% (6%), GLUT2 by 40% (11%), SLFN12 by 61% (14

29 LP-1 system by pharmacological inhibition of DPP-4 caused hyperinsulinemia, suppression of glucagon r

30 opeptidases, such as dipeptidyl peptidase-4 (DPP-4, CD26), are potent therapeutic targets for pharmac

31 ecific dipeptidyl aminopeptidase IV (DPP IV, DPP-4, CD26), widely expressed in mammalians, releases X

32 ully active CXCR3 agonists, yet resistant to DPP-4 cleavage.

33 nyl-, and peptidyl-Gly-Pro substrates, which DPP-4 cleaved poorly, suggesting an N-acyl-Gly-Pro motif

34 GLP-1 signaling is unclear, however, because DPP-4 cleaves other molecules as well.

35 f integrin beta1 and dipeptidyl peptidase-4 (DPP-4) compared with gMDSCs as part of an enhanced cell

36 Dipeptidyl peptidase 4 (DPP-4) degrades the incretin hormones glucagon-like pept

37 rescriptions for GLP-1RAs (reference group), DPP-4 (dipeptidyl peptidase 4) inhibitors (DPP-4is), SGL

38 (sodium-glucose cotransporter-2) inhibitors, DPP-4 (dipeptidyl peptidase-4) inhibitors, sulfonylureas

39 alues for other prolyl peptidases, including DPP-4, DPP-7, DPP-8, DPP-9, prolyl oligopeptidase, and a

40 ion of compounds 34b and 46b in complex with DPP-4 enzyme revealed that (R)-stereochemistry at the 8-

41 ed as inhibitors of dipeptidyl peptidase IV (DPP-4) for the treatment of type 2 diabetes.

42 rmation of conserved residues FAP Glu204 and DPP-4 Glu206.

43 olyl peptidases like dipeptidyl peptidase-4 (DPP-4) have not been developed.

44 ts and inhibitors of dipeptidyl peptidase-4 (DPP-4) have shown pleiotropic effects on bone metabolism

45 are both cleaved by dipeptidyl peptidase-4 (DPP-4); hence, inhibition of DPP-4 activity enables yet

46 ent in vitro potency (IC50 = 4.3 nM) against DPP-4, high selectivity over other enzymes, and good pha

47 o had baseline serum dipeptidyl peptidase-4 (DPP-4) higher than the population baseline median, we no

48 Targeting DPP-4 in mMDSCs reduced pERK signaling and their migrati

49 In vitro and in vivo assays of DPP-4 inhibition (DPP-4i) on monocyte activation/migrati

50 These studies suggest that DPP-4 inhibition ameliorates hepatic steatosis and insul

51 This study provides evidence that both DPP-4 inhibition and sulfonylurea reverse T2D-induced BB

52 The cardiovascular mechanisms engaged by DPP-4 inhibition are more complex, encompassing increase

53 -MS), antioxidant capacity (ORAC, ABTS), and DPP-4 inhibition assays.

54 iptin increased intact GLP-1 and GIP through DPP-4 inhibition but reduced total GLP-1 and GIP (feedba

55 oved beta-cell function by 37 +/- 12% during DPP-4 inhibition by sitagliptin.

56 This suggests that DPP-4 inhibition has the potential to reduce cardiovascu

57 DPP-4 inhibition mechanism by the peptides was investiga

58 rimary aims were to determine the effects of DPP-4 inhibition on GLP-1 clearance and on hepatic gluco

59 blockade, whereas the inhibitory effects of DPP-4 inhibition on glucagon and GE were abolished.

60 blood glucose is impaired; 2) the effect of DPP-4 inhibition on glycemia is likely to depend on adeq

61 DPP-4 inhibition reduced glycemia and enhanced insulin l

62 Furthermore, DPP-4 inhibition rescued WD-induced decreases in hepatic

63 antagonist, the glucose-lowering effects of DPP-4 inhibition were reduced by approximately 50%.

64 (PEP2) and QLRDIVDK (PEP4) displayed potent DPP-4 inhibition with IC50 values of 73.5, 82.5 and 8.55

65 DPP-4 inhibition with saxagliptin did not increase or de

66 strongly preferred over (S) with respect to DPP-4 inhibition.

67 improved beta-cell function observed during DPP-4 inhibition.

68 significantly to the therapeutic effects of DPP-4 inhibition.

69 d discusses these nonclassical mechanisms of DPP-4 inhibition.

70 es GLP mediating the antidiabetic effects of DPP-4 inhibition.

71 lin excursion after an OGTT with and without DPP-4 inhibition.

72 pic effects may contribute to the effects of DPP-4 inhibition.

73 erapeutic effects of dipeptidyl peptidase 4 (DPP-4) inhibition (vildagliptin) by using the GLP-1 rece

74 4 patients with T2D, dipeptidyl peptidase-4 (DPP-4) inhibition and its glucose-lowering actions were

75 GAT1 inhibition with dipeptidyl-peptidase-4 (DPP-4) inhibition led to further enhancements in active

76 genous GLP-1 through dipeptidyl peptidase 4 (DPP-4) inhibition.

77 ed to vehicle or alogliptin, a high-affinity DPP-4 inhibitor (40 mg . kg(-1) . d(-1)), for 12 weeks.

78 e medication (aHR, 1.12; 95% CI, 1.08-1.16), DPP-4 inhibitor (aHR, 1.18; 95% CI, 1.11-1.26), or sulfo

79 enyl)butanamide (6), a potent, orally active DPP-4 inhibitor (IC(50) = 6.3 nM) with excellent selecti

80 er 1000 person years, respectively, versus a DPP-4 inhibitor (NNT of 16).

81 when an SGLT-2 inhibitor was compared with a DPP-4 inhibitor (rate ratio 0.73 (0.68 to 0.78), rate di

82 inedione (SMD, 0.16 [95% CI, 0.00 to 0.31]), DPP-4 inhibitor (SMD, 0.33 [95% CI, 0.13 to 0.52]), and

83 We then administered saline (control), or a DPP-4 inhibitor (valine pyrrolidide or sitagliptin) with

84 ion of the tricyclic structure of the potent DPP-4 inhibitor 1.

85 ovascular events were not increased with the DPP-4 inhibitor alogliptin as compared with placebo.

86 EXAMINE trial showed non-inferiority of the DPP-4 inhibitor alogliptin to placebo on major adverse c

87 r microenvironment, whereas treatment with a DPP-4 inhibitor extended survival in preclinical GBM mod

88 hesis of sitagliptin, a potent and selective DPP-4 inhibitor for the treatment of type 2 diabetes mel

89 ts included in the study, 26 578 were in the DPP-4 inhibitor group (14 443 [54.34%] male; mean [SD] a

90 years, 1.76), compared with 57 events in the DPP-4 inhibitor group (IR, 1.77) (HR, 0.98 [95% CI, 0.68

91 The DPP-4 inhibitor prevented WD-induced hepatic steatosis a

92 human GLP-1 analogue liraglutide versus the DPP-4 inhibitor sitagliptin, as adjunct treatments to me

93 us (HIV) infection during treatment with the DPP-4 inhibitor sitagliptin.

94 tion of endogenous GIP to the effects of the DPP-4 inhibitor sitagliptin.

95 liraglutide versus a hypocaloric diet or the DPP-4 inhibitor sitagliptin.

96 role in health and improve the precision of DPP-4 inhibitor therapies.

97 thiazolidinedione, an SGLT-2 inhibitor, or a DPP-4 inhibitor to metformin to improve glycemic control

98 iated with a lower rate of hyperkalemia than DPP-4 inhibitor treatment (hazard ratio 0.75, 95% confid

99 (5.6 +/- 1.7 mmol/mol) lower A1C response to DPP-4 inhibitor treatment in G-allele carriers, but ther

100 ay, development of diabetes, and response to DPP-4 inhibitor treatment.

101 G) content was significantly attenuated with DPP-4 inhibitor treatment.

102 ates of in-hospital heart failure in another DPP-4 inhibitor trial have been reported.

103 of 10,089 propensity score-matched pairs of DPP-4 inhibitor users and sulfonylurea users were examin

104 de, which might be useful in the creation of DPP-4 inhibitor's design strategies.

105 f exenatide (GLP-1 agonist) and sitagliptin (DPP-4 inhibitor) during periodontitis induction by ligat

106 Treatment with a DPP-4 inhibitor, alogliptin (AG), significantly reduced

107 half the effect seen with the addition of a DPP-4 inhibitor, and equated to a dose difference of 550

108 ose Western diet (WD) or a WD containing the DPP-4 inhibitor, MK0626, for 16 weeks.

109 sed imidazopyridine dipeptidyl peptidase IV (DPP-4) inhibitor 1 has been developed.

110 ptor agonist, with a dipeptidyl peptidase-4 (DPP-4) inhibitor as alternative comparator.

111 as as effective as a dipeptidyl peptidase-4 (DPP-4) inhibitor at reducing peak glucose levels in an a

112 Linagliptin is a dipeptidyl peptidase-4 (DPP-4) inhibitor in clinical use against type 2 diabetes

113 caloric diet, or the dipeptidyl peptidase 4 (DPP-4) inhibitor sitagliptin.

114 Linagliptin is a dipeptidyl Peptidase-4 (DPP-4) inhibitor that inhibits the degradation of glucag

115 potent and selective dipeptidyl peptidase 4 (DPP-4) inhibitor with an excellent pharmacokinetic profi

116 uding saxagliptin, a dipeptidyl peptidase 4 (DPP-4) inhibitor, are unclear.

117 associated with lower mortality compared to DPP 4 inhibitors and lower costs compared to GLP-1 agoni

118 al admission for heart failure compared with DPP-4 inhibitors (0.32, 0.12 to 0.90) and sulfonylureas

119 rtainty in the estimated hazard ratio versus DPP-4 inhibitors (0.64, 0.29 to 1.43).

120 iated with a lower rate of hyperkalemia than DPP-4 inhibitors (0.79, 0.77 to 0.82).

121 per 1000 person-years) and in 1141 users of DPP-4 inhibitors (15.4 per 1000 person-years; hazard rat

122 1% to 2.7%) lower for SGLT-2 inhibitors than DPP-4 inhibitors (4.6% v 7.0%), 1.8% (1.4% to 2.1%) lowe

123 2.1%) lower for GLP-1 receptor agonists than DPP-4 inhibitors (5.7% v 7.5%), and 1.2% (0.9% to 1.5%)

124 e initiating use of SGLT-2 inhibitors versus DPP-4 inhibitors (cohort 1) or GLP-1 agonists (cohort 2)

125 DPP-4 inhibitors (DPP-4i) and sulphonylureas remain the

126 8; 95% confidence interval [CI], 1.30-6.80), DPP-4 inhibitors (IRR, 2.45; 95% CI, 1.54-3.89), sulfony

127 Compared with the use of DPP-4 inhibitors (n = 1,641,520), use of GLP-1 RAs (n =

128 ists (n = 448), SGLT-2 inhibitors (n = 112), DPP-4 inhibitors (n = 435), sulfonylureas (n = 2,253), o

129 atment with sulfonylureas (n=25 693, 33.9%), DPP-4 inhibitors (n=34 464 ,45.5%), or SGLT-2 inhibitors

130 ews the most recent CV outcome trials of the DPP-4 inhibitors (SAVOR-TIMI 53, EXAMINE, and TECOS) as

131 advances that reveal how GLP-1R agonists and DPP-4 inhibitors affect the normal and diabetic heart an

132 0.74-0.90]; P < 0.001), and continued use of DPP-4 inhibitors after hospitalization was associated wi

133 The results were similar for DPP-4 inhibitors and GLP-1 analogues.

134 of anaphylactic reaction when compared with DPP-4 inhibitors and SGLT-2 inhibitors.

135 DPP-4 inhibitors do not lower postprandial glucose conce

136 es demonstrate that both GLP-1R agonists and DPP-4 inhibitors exhibit cardioprotective actions in ani

137 DPP-4 inhibitors expand beta-cell mass, reduce alpha-cel

138 ay provide an impetus for the development of DPP-4 inhibitors for the prevention and treatment of str

139 nd metformin-based combinations, except that DPP-4 inhibitors had smaller effects.

140 DPP-4 inhibitors improve glycemic control in type 2 diab

141 rs were more effective than sulfonylureas or DPP-4 inhibitors in lowering mean HbA(1c), BMI, and syst

142 rs were more effective than sulfonylureas or DPP-4 inhibitors in reducing BMI and systolic blood pres

143 iated with a lower risk of hyperkalemia than DPP-4 inhibitors in the overall population and across re

144 ox models with exposure to sulfonylureas and DPP-4 inhibitors included as time-varying covariates wer

145 The classical mechanism for DPP-4 inhibitors is that they inhibit DPP-4 activity in

146 SGLT-2 inhibitors were more effective than DPP-4 inhibitors or sulfonylureas in reducing mean HbA(1

147 ith 73% lower mortality compared to those of DPP-4 inhibitors or users of older agents, while 36% low

148 senatide in Acute Coronary Syndrom]) and the DPP-4 inhibitors saxagliptin (SAVOR-TIMI 53 trial [Saxag

149 The risk for hHF was not higher with DPP-4 inhibitors than with the other study drugs.

150 humans have found additional mechanisms for DPP-4 inhibitors that may contribute to their glucose-lo

151 effects on cardiovascular outcomes of adding DPP-4 inhibitors versus sulfonylureas to metformin thera

152 Use of DPP-4 inhibitors was associated with a reduction in resp

153 DPP-4 inhibitors were associated with lower risks for al

154 Compared with sulfonylureas, DPP-4 inhibitors were associated with lower risks for al

155 DPP-4 inhibitors were selected as the comparator due to

156 In our effort to discover DPP-4 inhibitors with added benefits over currently comm

157 gment with B-aminobutanoyl linker, and (iii) DPP-4 inhibitors with pyrimidine-2,4-dione or analogs as

158 s of hospital admission for heart failure (v DPP-4 inhibitors) and kidney disease progression (v sulf

159 xposed to sulfonylureas was 9.7% (n = 1362); DPP-4 inhibitors, 6.1% (n = 687); GLP-1 receptor agonist

160 Metformin was more efficacious than the DPP-4 inhibitors, and compared with thiazolidinediones o

161 on or after May 1, 2016: SGLT-2 inhibitors, DPP-4 inhibitors, GLP-1 agonists or older agents (metfor

162 ht was reduced or maintained with metformin, DPP-4 inhibitors, GLP-1 receptor agonists, and SGLT-2 in

163 -1.46) for infants exposed to sulfonylureas, DPP-4 inhibitors, GLP-1 receptor agonists, and SGLT2 inh

164 nefits over currently commercially available DPP-4 inhibitors, MK-3102 (omarigliptin), was identified

165 lating medications, such as GLP-1R agonists, DPP-4 inhibitors, or pioglitazone, may improve COVID-19

166 Compared with DPP-4 inhibitors, SGLT-2 inhibitors were associated with

167 Compared with DPP-4 inhibitors, the lower rate of hyperkalemia was con

168 Compared with use of DPP-4 inhibitors, use of liraglutide was associated with

169 use of liraglutide, as compared with use of DPP-4 inhibitors, was associated with significantly redu

170 receipt of SGLT-2 inhibitors with receipt of DPP-4 inhibitors, which were pooled by using random-effe

171 rt included incident users of liraglutide or DPP-4 inhibitors, who were also using metformin at basel

172 ardiovascular actions of GLP-1R agonists and DPP-4 inhibitors, with a focus on the translation of mec

173 l propensity scores to 208 757 recipients of DPP-4 inhibitors.

174 mpared with pioglitazone, sulfonylureas, and DPP-4 inhibitors.

175 (-4.6 to -1.8) for SGLT-2 inhibitors versus DPP-4 inhibitors.

176 receptor agonists and patients treated with DPP-4 inhibitors.

177 sulfonylureas and 0.91 (0.51 to 1.63) versus DPP-4 inhibitors.

178 d with GLP-1 receptor agonists compared with DPP-4 inhibitors.

179 Initiation of GLP-1 RAs compared with DPP-4 inhibitors.

180 ceptor agonists compared with treatment with DPP-4 inhibitors.

181 -stage CKD, and ESKD than was treatment with DPP-4 inhibitors.

182 s of liraglutide and 23 402 matched users of DPP-4 inhibitors; patients were followed up for a mean o

183 sed drugs, including dipeptidyl peptidase 4 (DPP-4) inhibitors and glucagon-like peptide 1 (GLP-1) an

184 roups (initiators of dipeptidyl peptidase 4 (DPP-4) inhibitors and initiators of sodium-glucose cotra

185 Dipeptidyl peptidase-4 (DPP-4) inhibitors are commonly used antidiabetic agents

186 Dipeptidyl-peptidase 4 (DPP-4) inhibitors are increasingly used to accomplish gl

187 eceived GLP-1 RAs or dipeptidyl peptidase-4 (DPP-4) inhibitors between 2011 and 2022 were identified.

188 rated CV safety of 3 dipeptidyl peptidase 4 (DPP-4) inhibitors but have included limited numbers of p

189 , and orally active dipeptidyl peptidase IV (DPP-4) inhibitors by extensive structure-activity relati

190 Dipeptidyl peptidase-4 (DPP-4) inhibitors have pleotropic anti-inflammatory and

191 In this regard, dipeptidyl peptidase-4 (DPP-4) inhibitors have recently been reported to attenua

192 -1 activity, whereas dipeptidyl peptidase-4 (DPP-4) inhibitors increase concentrations of endogenous

193 glucose lowering by dipeptidyl peptidase-4 (DPP-4) inhibitors is unclear.

194 Dipeptidyl peptidase-4 (DPP-4) inhibitors prevent degradation of incretin hormon

195 udies concluded that dipeptidyl peptidase-4 (DPP-4) inhibitors provide glycemic control but also rais

196 GLP-1R) agonists and dipeptidyl peptidase-4 (DPP-4) inhibitors represent 2 distinct classes of incret

197 and potent reported dipeptidyl peptidase-4 (DPP-4) inhibitors with gliptin-like structures are class

198 r (GLP-1R) agonists, dipeptidyl peptidase 4 (DPP-4) inhibitors, and pioglitazone, are known to have a

199 ones, sulfonylureas, dipeptidyl peptidase-4 (DPP-4) inhibitors, and sodium-glucose cotransporter-2 (S

200 hHF) associated with dipeptidyl peptidase-4 (DPP-4) inhibitors, creating uncertainty about the safety

201 ll of sulfonylureas, dipeptidyl peptidase 4 (DPP-4) inhibitors, glucagon-like peptide 1 (GLP-1) recep

202 mparator drug class, dipeptidyl peptidase-4 (DPP-4) inhibitors, in patients with type 2 diabetes.

203 or (GLP-1) agonists, dipeptidyl peptidase 4 (DPP-4) inhibitors, peroxisome proliferator-activated rec

204 edication, including dipeptidyl peptidase-4 (DPP-4) inhibitors, sodium-glucose cotransporter 2 (SGLT2

205 ists (GLP-1 RAs) and dipeptidyl peptidase-4 (DPP-4) inhibitors, which inhibit the physiological inact

206 thiazolidinediones, dipeptidyl peptidase 4 [DPP-4] inhibitors, glucagon-like peptide 1 [GLP-1] recep

207 ncer drug mitoxantrone possesses significant DPP-4 inhibitory activity both in vitro and in vivo.

208 his method to screening drugs with potential DPP-4 inhibitory activity.

209 eeds are an adequate source of peptides with DPP-4 inhibitory properties that could be used in functi

210 gastrointestinal digestion were studied for DPP-4 inhibitory properties using in vitro and in situ a

211 Binding of gliptins to DPP-4 is a rapid electrostatically driven process.

212 Because DPP-4 is expressed in inflammatory cells, we hypothesize

213 od was collected for analysis of glucose and DPP-4 levels.

214 which inhibitors of dipeptidyl peptidase-4 (DPP-4) lower postprandial glucose concentrations.

215 perties, research on gut microbially derived DPP-4 (mDPP-4) remains limited.

216 -36), a cardioactive metabolite generated by DPP-4-mediated cleavage.

217 the peptides either block the active site of DPP-4 or changes the enzyme conformation via a secondary

218 Vildagliptin fully inhibited DPP-4 over the 4-h experimental period.

219 ion by inhibition of dipeptidyl peptidase-4 (DPP-4) promotes glycemic reduction for the treatment of

220 subsets and suggest that integrin beta1 and DPP-4 represent putative immunotherapy targets to attenu

221 To develop a DPP-4-resistant variant, we combined biochemical analysi

222 Thus, a significant DPP-4-sensitive glucose-lowering mechanism contributes t

223 e, Pro, or Arg at the P(2) residue; however, DPP-4 showed broad reactivity against this library, prec

224 ibrary, FAP cleaved only Ac-Gly-Pro, whereas DPP-4 showed little reactivity with all substrates.

225 unclear, and it is unknown whether conserved DPP-4 substrate binding residues support FAP endopeptida

226 eview connects ongoing discussions regarding DPP-4 substrate specificity and potential access routes

227 e CP-induced increase in the levels of other DPP-4 substrates such as stromal cell-derived factor-1 a

228 DPP-4 was highly expressed in bone marrow-derived CD11b(

229 ed by the action of dipeptidyl peptidase IV (DPP-4) which limits their use as therapeutic agents.

230 s, and inhibition of dipeptidyl peptidase-4 (DPP-4), which cleaves GLP-1, is renoprotective in rodent

231 The peptides bound to DPP-4 with micromolar affinities and PEP4 showed signifi

232 Whether inhibition of DPP-4 with sitagliptin may prevent acute GVHD after allo